Chapter 9 Kidney Disease Flashcards
Diagnosis and screening to determine kidney diseases
- Abnormality in biochemical blood screen
- functional change in glomerular filtration rate (GFR)
- abnormality in urinalysis: proteinuria and hematuria
- systemic disease with renal involvement: diabetes mellitus
- symptom, physical sign, imaging
- kidney biopsy
Major types based on where kidney was initially affected
- Glomerular
- Tubular
- Interstitial
- Vascular
What major type is most often immune related?
Glomerular
What major type affects proximal/distal tubules and is a result from toxic or infectious substances
Tubular
What major type is damage from neglected UTIs and result from toxic or infectious substances
Interstitial
What major type affects blood flow from the heart and reduces renal perfusion?
Vascular
Types of glomerular disorders and morphologic changes
Distinct changes/damage: - immunologic - non-immunologic Types: - primary immunologic - Secondary to systemic diseases - hereditary
Immune mediated changes in glomerulus
- Cellular proliferation: increased numbers of endothelial and other cells
- Leukocyte infiltration
- glomerular basement membrane thickening: immune complexes and diabetes
- Hyalinization with sclerosis (scarring)
Clinical features of nephritis vs nephrotic diseases
- Hematuria
- proteinuria
- Lipiduria
- oliguria
- Azotemia (increased blood urea nitrogen)
- Edema
- Hypertension
2 glomerular diseases
Nephritic and nephrotic: acute, chronic
Features of nephrotic syndrome
- Onset: insidious
- Edema: ++++
- Blood pressure: normal
- jugular venous pressure:normal/low
- Proteinuria: ++++
- Hematuria: may/may not occur
- red blood cell casts: absent
- serum albumin: low
Features of nephritic syndrome
- Onset: abrupt
- edema: ++
- blood pressure: raised
- jugular venous pressure: raised
- proteinuria: ++
- hematura: +++
- Red blood cell casts: present
- serum albumin: normal/ slightly reduced
Cause of nephrotic syndrome
Increased permeability of the glomerular due to damage of basal Lamina and podocytes. Massive loss of protein (mostly albumin) in urine
Clinical findings of nephrotic syndrome
Pronounced soft and pitting edema and hyperlipidemia
Urinalysis of nephrotic syndrome
Cloudy, fat droplets
- protein > 3.5g/day and 4+ positive on dipstick
- lipiduria
- oily
Microscopic findings of nephrotic syndrome
- Oval fat bodies, free fat globes
- increased renal tubular epithelial cells
- increased casts: all types, particularly fatty, waxy, and renal well
Cause of acute post streptococcal glomerutonephritis
Sudden onset occurs 1-2 weeks after group A beta-hemolytic strep with M protein infection of throat or skin (strep throat)
Clinical findings of acute post streptococcal glomerulonephritis
Fever, edema, fatigue, hypertension, Algeria, hematuria
Urinalysis of acute post streptococcal glomerulonephritts
Cloudy, red or brown
- protein ( = casts), blood ( increased ASO titer and BUN), leukocyte esterase positive (need to look at in microscopic)
Microscopic findings of acute Post streptococcal glomerulonephritis
- Increased RBCs, often dymorphic
- Increased WBCs
- increased renal tubular epithelial cells
- Increased casts: RBC, hemoglobin, granular
Normal glomerulus
Post strep glomerulus
Rapidly progressive crescentric (acute nephritic)
- Cellular proliferation in Bowman’s space form crescents: leukocyte infiltration; fibrin deposits; damages to glomerular basement membrane
- Complication of systemic lupus erythematosis
Minimal change disease (acute nephrotic)
Loss of podocyte foot processes; dysfunction of t-cell immunity; follows infections and responsible for most cases of nephrotic syndrome in children; rapid response to steroids
Focal glomerulosclerosis (variable)
Sclerotic damage to limited number of glomeruli with hyaline and lipid deposits and loss of foot processes; focal IgM and C3 deposits. Proteinuria predominant